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dc.contributor.authorPan, Bin
dc.contributor.authorChen, Minjie
dc.contributor.authorZhang, Xuan
dc.contributor.authorLiang, Shuai
dc.contributor.authorQin, Xiaobo
dc.contributor.authorQiu, Lianglin
dc.contributor.authorCao, Qi
dc.contributor.authorPeng, Renzhen
dc.contributor.authorTao, Shimin
dc.contributor.authorLi, Zhouzhou
dc.contributor.authorZhu, Yaning
dc.contributor.authorKan, Haidong
dc.contributor.authorXu, Yanyi
dc.contributor.authorYing, Zhekang
dc.date.accessioned2020-12-10T14:45:04Z
dc.date.available2020-12-10T14:45:04Z
dc.date.issued2021-01-15
dc.identifier.urihttp://hdl.handle.net/10713/14231
dc.description.abstractAmbient fine particulate matter (PM2.5) exposure correlates with adverse cardiometabolic effects. The underlying mechanisms have not yet been fully understood. Hypothalamic-pituitary-adrenal (HPA) axis, as the central stress response system, regulates cardiometabolic homeostasis and is implicated in the progression of various adverse health effects caused by inhalational airborne pollutant exposure. In this study, we investigated whether ambient PM2.5 exposure activates HPA axis and its effect mediating PM2.5-induced pulmonary inflammation. C57Bl/6 J mice were intratracheally instilled with different concentrations of diesel exhaust PM2.5 (DEP), and plasma was harvested at different times. Assessments of plasma stress hormones revealed that DEP instillation dose- and time-dependently increased mouse circulating corticosterone and adrenocorticotropic hormone (ACTH) levels, strongly supporting that DEP instillation activates HPA axis. To determine which components of DEP activate HPA axis, C57Bl/6J mice were intratracheally instilled with water-soluble and -insoluble fractions of DEP. Plasma analyses showed that water-insoluble but not -soluble fraction of DEP increased circulating corticosterone and ACTH levels. Consistently, concentrated ambient PM2.5 (CAP) exposure significantly increased mouse urine and hair corticosterone levels, corroborating the activation of HPA axis by ambient PM2.5. Furthermore, deletion of stress hormones by total bilateral adrenalectomy alleviated PM2.5-induced pulmonary inflammation, providing insights into the contribution of central neurohormonal mechanisms in modulating adverse health effects caused by exposure to PM2.5.en_US
dc.description.urihttps://doi.org/10.1016/j.ecoenv.2020.111464en_US
dc.language.isoenen_US
dc.publisherElsevier Ltd.en_US
dc.relation.ispartofEcotoxicology and Environmental Safetyen_US
dc.rightsCopyright © 2020 Elsevier Inc. All rights reserved.en_US
dc.subjectHPA axisen_US
dc.subjectPM(2.5)en_US
dc.subjectPulmonary inflammationen_US
dc.subjectStress hormonesen_US
dc.titleHypothalamic-pituitary-adrenal axis mediates ambient PM exposure-induced pulmonary inflammation.en_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.ecoenv.2020.111464
dc.identifier.pmid33075589
dc.source.journaltitleEcotoxicology and environmental safety
dc.source.volume208
dc.source.beginpage111464
dc.source.endpage
dc.source.countryNetherlands


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